Sudden cardiac death usually secondary to ventricular fibrillation remains a major cause of mortality in the United States. Ventricular fibrillation is generally believed to be secondary to reentry; however, several aspects of the pathophysiology of ventricular fibrillation remain unknown. In particular, how the arrhythmia may differ in different experimental or clinical situations and whether activation during ventricular fibrillation is organized in a quantifiable fashion has not been well established. The overall goal of the present study is to verify the hypothesis that ventricular fibrillation is due to multiple reentrant circuits that change over time and that patterns of the initiation and maintenance of ventricular fibrillation may vary depending upon underlying structural or electrophysiologic properties of the myocardium and depending upon the mode of initiation of models of subacute and chronic myocardial infarction and dilated cardiomyopathy. Activation during ventricular fibrillation will be recorded using a computerized multi-channel mapping system and analyzed using standard activation mapping and "vector mapping" techniques. The size of activation wavefronts, the cycle length of fibrillation, the beat to beat organization of activation (spatial and temporal linking), the number and types of reentrant circuits and the location of lines of functional block will be used to characterize fibrillation. Refractory period measurements and pathologic analysis will also be performed and correlated with electrical activation during ventricular fibrillation. The specific hypotheses to be tested are: l) the mechanism of initiation and perhaps the maintenance of ventricular fibrillation will differ depending upon the method used to induce the arrhythmia; 2) patterns of activation during VF will vary depending on the experimental model and based on pre-existing local electrophysiologic and anatomic properties; 3) characteristics of VF (spatial and temporal linking, cycle length, and size of wavefronts) will vary as the duration of fibrillation increases; and 4) ventricular fibrillation is due to multiple simultaneous reentrant circuits. The number and characteristics of these circuits will vary depending upon the experimental situation and will be dependent upon of local electrophysiologic and anatomic properties of the myocardium. A better understanding of the pathophysiology of ventricular fibrillation and how it differs in different situations may lead to better therapies for the prevention and termination of this lethal arrhythmia.